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MMI133_Lecture12 Flashcards

1
Q

pathogen

A

microorganism that can cause a disease process

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2
Q

primary pathogens always

A

cause disease - even in healthy immuno-competant individs

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3
Q

opportunistic pathogen

A

microorganism that may cause disease if given the right circumstances

Candida albicans - immunosuppression
Mucor spp - diabetics
Pseudomonas aeruginosa - burns, CF, HIV, + neutropenic cancer patients

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4
Q

pathogenicity

A

ability to cause disease by evading or overcoming the host defences

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5
Q

virulence

A

extent to which the microorganism is pathogenic

how much disease it can cause

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6
Q

virulence factors

A

molecs/structures produced by pathogens that contribute to their pathogenicity or ability to cause disease

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7
Q

virulence factor of Streptococcus pneumoniae

A

capsule
cannot cause disease without capsul

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8
Q

portals of entry

A

how pathogen gains entry to host

mucous membranes
skin
parenteral route via mouth
surgical sites + implants can provide route to bypass these
some have preferred protal of entry + can only cause disease thru specific route

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9
Q

tropism

A

a liking of an organism for a certain cell or tissues

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10
Q

tropism is determined by

A

distribution of cell receptors for microbes
accessibility of correct host cell types
other competing microbes
nut.s for growth
physical + innate difenses at the site of infection + age
permissive environmental condition like pH

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11
Q

some pathogens can

A

remain at site of infection + don’t have to spread thru system to cause disease

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12
Q

exotoxin producing bacteria

A

corynebacterium diphtherieae
vibrio cholerae
clostridium tetani, botulinum, perfringens
bordetella pertussis

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13
Q

first step of infection

A

adherence + binding

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14
Q

pathogens adhere + bind in infection by

A

adhesins/ligands (pathogen structures) recognizing + binding to receptors on host cells

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15
Q

adhesins = ligands

A

structures on pathogens that bind to host receptor in adherence step of infection

most on pathogens are glycoproteins or lipoproteins

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16
Q

receptors

A

strucutres on host cells that adhesins/ligands bind to when pathogen binds to host cell

most are sugars like mannose

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17
Q

factors that help bact evade + penetrate host defenses

A

capsules
cell wall compenents
biofilms
enzymes
invasins
superantigens
toxins
secretion systems
antigenic variation
intra/extracellular growth

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18
Q

capsules

A

glycocalyx = capsule + slime layer etc

initially prevents phagocyte from recognizing + binding to + ingesting bact

many can in right conditions

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19
Q

cell wall compenents

A

fc receptors on microorganisms prevent opsonization

fc’s covered up by cell wall compenents so phagocytes can’t eat them

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20
Q

M protein

A

heat + acid-resistant protein in cell wall that allows attachment of bact to epithelial cells + inhibits phagocytosis

Streptococcus pyogenes

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21
Q

Mycolic acids

A

waxy substance in cell walls make bact resistant to digestion inside phagocyte

Mycobacterium tuberculosis

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22
Q

biofilms

A

united we stand for bact

community of bact surrounded often by shared glycocalyx
reduced antibiotic effectiveness WBC penetration

bad in medical implants

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23
Q

exoenzymes released form bact cells

A

leucocidin - destroys WBC
kinase - breaks down fibrin + dissolves clots formed by body to isolate infection
hemolysin - break down RBC

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24
Q

coagulase

A

clots - converts fibrinogen (soluble in plasma) to fibrin protein strands which clot and can wall bact off from host defeneses

Staphylocuccs aureus

25
collagenase
breaks donw collagen CT clostridium perfringens
26
lecithinase
destroy PM's clostridium perfringens
27
proteases
inactivate antibiotics + other body proteins like IgA protease neisseria gonorrhoeae
28
coagulase test
plasma with bact is incubated and there's soluble fibrinogen in the plasma after incubation, if it's positive for coagulase then it will clot bec coagulase will clot the blood, if it doesn't clot then -, bec it's not turned to fibrin by coagulase
29
invasins
surface proteins on some bact which activate actin - the cytoskeleton eukaryotic cells rearranges + facilitates bact engulfment into host cell
30
superantigens
type 1 exotoxins protein antigens that stimulate super large immune response instead of <1% Th cell activation in normal antigens, it causes 20% Th cell activation unspecific binding to MHC II + TCR results in excessive cytokine release immune system works against us bipass keep to act, not lock and key antigen, but a master key antigen
31
toxins
often primary virulence factor usually proteins that produce fever + cause heart failure, diarrhea, edema or shock can destroy cells endotoxin - LPS lipid A - molec contributes to bact structure exotoxin - incl superantigens - extra protein made by bact to affect cells other than itself
32
endotoxins
ONLY G- bact lipopolysaccharide LPS) + lipid A heat stable
33
shock
life-threatening loss of BP
34
septic shock
shock caused by any bact
35
endotoxic shock
shock caused by G- bact
36
streptococcus pneumoniae
G+ diplococcus
37
exotoxins
proteins certain bact make + release into tissues G+ + G- genes for exotoxins carried by bacteriophages or plasmids diphtheria toxin, tetanus toxin Cytotoxin - cell neurotoxin - nerves enterotoxin - intestines heat labile/sensitive to heat antitoxin antibodies for neutralization
38
exotoxin-caused diseases
botulism tetanus gas gangrene diphtheria whooping cough listeriosis cholera
39
Clostridium botulinum
causes flaccid paralysis due to botulism toxin
40
Clostridium tetani
causes spastic paralysis = lockjaw, due to tetanus toxin
41
pathogenicity island
chromosomal region where the genes are clustered
42
type III apparatus enables
a bact cell to inject proteins into a host cell, killing or altering it
43
antigenic variation
escaping immune system by changing their antigens some pathogens change the makeup of their antigens as they replicate/mutate and immune system sees them as new pathogens creates new antigen by the time host has created antibodies to first one
44
obligate intracellular bacteria
can only grow inside of host cells, often in protected vacuole
45
facultative intracellular bacteria
can multiply outside host cells, but often use intracellular growth as means of evading host defenses Bordetella, mycobacterium, Salmonella
46
Hemolysin will
not help pathogens avoid immune detection
47
3 methods of horizontal gene transmission
conjugation transduction transformation
48
conjugation
transferral of plasmids containing genes for virulence attributes or antibiotic resistance
49
transduction
acquisition of genes for toxin production eg. C. diphtheriae bact via transferral by bacteriophage
50
transformation
acquiring gene for toxin, capsule production etc, by absorbing naked DNA from environment arnd bacterium
51
plasmid
small circular DNA molecs separated from main bacterial chromosome encode antimicrobial resistance or virulence factors
52
bacteriophages
viruses which infect specific bacteria transfer genes by transduction
53
what is name for 2 live bacterial cells directly passing DNA betw each other
conjugation
54
most effects of viral infections caused by
inflammation + activation of immune system producing disease
55
cytopathic effects CPE
kiilling or damaging of host cell diff strains of virus cause diff CPE
56
syncytium formation
infected cells fuse to form giant cell with many nuclei giant virus producing factory giant cell dies when viruses use up all building material + cause necrosis of tissue permits viral multiplication without exposing virus to antibodies
57
syncytium
mega infected virus-hyjacked cell virus making factory
58
viral pathogenicity - what can viruses do to cause disease?
evade immunity with syncytium + make face MHC I disrupt cellular life cycle + activity can cause cancer - induce chromosomal changes in cells oncoviruses, deregulate contact inhibition so cell growth doesn't stop when runs out of space
59
what is a common thing betw bact + some viruses
can replicate intracellularly

MMI133 (16 decks)

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